机构地区:[1]NationalLaboratoryofMolecularOncology,DepartmentofThoracicSurgeryandDepartmentofPathology,CancerInstituteandHospital,ChineseAcademyofMedicalSciencesandPekingUnionMedicalCollege,Beijing100021,China [2]QiluHospital,SchoolofMedicine,ShandongUniversity,Qindao250012,ShandongProvince,China [3]BeijingYanjingHospital,Beijing100037,China
出 处:《World Journal of Gastroenterology》2004年第10期1387-1391,共5页世界胃肠病学杂志(英文版)
基 金:Supported by National Natural Science Foundation,No.30225045,No.39990570,No.30171049 and No.30370713,and National High Tech and Major State Basic R & D Program of China,No.G 1998051205and No.2001AA227091
摘 要:AIM: To investigate biogenesis and intracellular Iocalizations of clusterin to elucidate the potential molecular mechanisms implicated in tumorigenesis of esophageal mucosa.METHODS: Semi-quantitative RT-PCR for multi-region alteration analysis, Western blot for different transcriptional forms and immunohistochemical staining for intracellular Iocalizations of clusterin were carried out in both tissues and cell lines of ESCC.RESULTS: The N-terminal deletions of the clusterin gene and the appearance of a 50-53 ku nuclear clusterin, an uncleaved, nonglycosylated, and disulfide-linked isoform,were the major alterations in cancer cells of esophagus.Naturally the 40 ku clusterin was located in the connective tissue of the lamina propria of epithelial mucosa and right under the basal membrane of epithelia, but it was disappeared in stromal mucosa of esophagus and the pre-matured clusterin was found positive in cancerous epithelia.CONCLUSION: The N-terminal deletion of clusterin may be essential for its alterations of biogenesis in ESCC.AIM:To investigate biogenesis and intracellular localizations of clusterin to elucidate the potential molecular mechanisms implicated in tumorigenesis of esophageal mucosa. METHODS:Semi-quantitative RT-PCR for multi-region alteration analysis,Western blot for different transcriptional forms and immunohistochemical staining for intracellular Iocalizations of clusterin were carried out in both tissues and cell lines of ESCC. RESULTS:The N-terminal deletions of the clusterin gene and the appearance of a 50-53 ku nuclear clusterin,an uncleaved,nonglycosylated,and disulfide-linked isoform, were the major alterations in cancer cells of esophagus. Naturally the 40 ku clusterin was located in the connective tissue of the lamina propria of epithelial mucosa and right under the basal membrane of epithelia,but it was disappeared in stromal mucosa of esophagus and the pre-matured clusterin was found positive in cancerous epithelia. CONCLUSION:The N-terminal deletion of clusterin may be essential for its alterations of biogenesis in ESCC.
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